Lvd Report Sample

Hypertrophic cardiomyopathy is an inherited autosomal-dominant pattern affecting nearly 1 in 500 people, affecting both men and women equally. Which makes it the most “common genetic heart disease in the United States” [5] Many studies have been done on the causes of this disease. Research has shown the mutations of between 10 to 13 sarcomeric proteins are associated with HCM. Each mutated gene has a different pathological characteristic.

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

Through more research, dilated cardiomyopathy has been found to have a genetic component (MacRae, 2010). Though there have been families who have volunteered to be screened, there are still some 40 chromosomal loci and potential disease genes discovered so far. The reason for the wide range of variants of potential loci is due to how prevalent the disease is in families. For example, the more individuals who have been diagnosed with the disease, researchers were then able to find similar loci among the affected; whereas, the families who had fewer affected individuals laid a wider range of

However, in the further with further increasing numbers of SV survivors, we will probably encounter CADs in SV patients. Nevertheless and more importantly, in SV patients who have received or will receive heart transplant an previously had IMAs embolization, IMAs CABG would not be available for them when they develop transplant coronary arterial (allograft) vasculopathy. Transplant coronary arterial (allograft) vasculopathy is of the foremost causes of morbidity and mortality after heart transplantation. Surgical (CABG) and transcatheter revascularization has been reported as a successful and viable treatment options in short as well as midterm follow up [26,27]. Therefore, losing IMAs will deprive those patients from the best graft to treat their

Dilated cardiomyopathy (DCM) is a disorder caused by abnormalities in functional regions of the heart muscle. [Maron et al., 2006] It is one of two major types of cardiomyopathies, the other being hypertrophic cardiomyopathy (HCM). In DCM the ventricles are dilated with dysfunctional systolic pressure, affecting 1 in 2500 individuals. [Codd et al., 1989, Pahl, 2010] Familial DCM is diagnosed when two or more family members die or there is sudden death of a child due to DCM. [Mestroni et al., 1999] The end point for DCM is heart failure. [Pahl, 2010] Mutations in over 30 genes have been identified as the main causes of familial and sporadic DCM (~ 33% of cases) [Gru ̈nig et al., 1998; Jefferies et al., 2010; Macara 2001; Michels et al., 1992;

antiviral medication (Al-Akchar et al., 2017). In the worst cases, mechanical support devices have been used, along with heart transplant surgeries (Al-Akchar et al., 2017). In conjunction with these treatment plans, patients are advised to limit exercise activities, and are recommended to have continuous echocardiography over the years to continue to ensure that the disease does not make a comeback (Al-Akchar et al., 2017). As it exists now, there is much to be desired in the diagnosis and treatment for myocarditis, let alone any of its subtypes. There is much to be learned from this mysterious disease, and although technology continues to advance, it may still be a long time until we can accurately diagnose and treat

At Harvard Universities ' Stem Cell Institute (HSCI), two researchers - Richard T. Lee and Amy Wagers – have discovered a protein found in both mouse and human blood that can reverse the effects of heart failure in the elderly. Richard T. Lee, a Harvard Medical School professor and cardiologist, has many patients of old age who suffer from diastolic heart failure. Amy Wagers, a stem cell biologist and Harvard professor, stresses that the protein, called GDF-11, may be the first effective treatment for the common heart failures that effect many Americans today.

After a heart attack, the heart is unable to regenerate cardiac muscle cells known as myocytes which diminishes the heart’s pump function. The heart tries to heal itself by changing the damaged or dead heart muscle cells into scar tissue. However, the scar tissue cannot function as a muscle so it does not contribute to the cardiac contractile force. Overtime, this leads to a greater burden on the remaining viable heart muscle which eventually leads to heart failure. Current treatments such as autologous grafting and commercially available fillers incur donor-site morbidity and volume loss over time. Other transplantation therapies do not directly address the loss of cardiac myocytes, which leads to the drive for more research in cardiac regeneration.

Familial Cardiomyopathies (FC) are a collection of cardiac diseases that vary vastly genetically, and pathologically (1, 2). Hypertrophic cardiomyopathy (HCM) is the most common form of FC (2). HCM is diagnosed often with left ventricular hypertrophy without a noticeable increase in external load and smaller ventricular cavity, but with a preserved ejection fraction (3). That is, the percent of blood leaving the left ventricle (5) does not change. Other pathologies include interstitial fibrosis, thickening of the media in intramural arteries, and myocytes disarray greater than 5%; which is a hallmark of HCM (4). HCM shows variability in its penetrance, from a patient with no symptoms, to having sudden cardiac death (SCD)

Left Ventricular Systolic Dysfunction (LVSD) is an abnormal cardiovascular symptom characterized by a reduction in the left ventricular ejection fraction (LVEF), a measurement of the percentage of blood leaving the heart with each contraction. LVEF is commonly measured using echocardiography and calculated as the ratio between the blood volume exiting the left ventricle over the volume filling the left ventricle. A higher ejection fraction (EF) indicates better strength and contractility of the heart. Recent guidelines from the American and European society of echocardiography have defined an abnormal LVEF as any EF <40-55%.

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This report has allowed us to have an exceptional understanding of LVADs and the advanced sonographic technique needed to fully evaluate its function. With this found knowledge, we can confidently enter an LVAD exam knowing what is required of us. Before a patient receives an LVAD, an important area to evaluate is the presence of aortic regurgitation and its severity. Post LVAD implant, we know to evaluate the aortic valve in more ways then one to assess any aortic valve opening. Also, the inflow and outflow cannulas need show flow as continuous and pulsatile to show no signs of

Investigations performed at the gene level delineate differences in the mRNA and miRNA protein gene expressions between the two ventricles, with higher levels of expression concentrated in LV 11. Other reports suggest differences at the protein levels of the two ventricles wherein higher amounts of energy using proteins like ATP synthase and others like Heat Shock Protein (HSP), Myosin Binding Protein C (MBPC) and Myosin Light Chain 2 (MLC2) were noted in Left compared to the Right ventricles in healthy mice hearts 5, 24, 38.

Myocardial infarction (MI) is the leading causes of mortality and morbidity in the world. Ischemic heart disease, where the oxygen supply to the myocardium is restricted, is a common cause of an MI. Myocardial injury results in loss of cardiomyocytes (cardiac muscle cells) due to apoptosis, and the development of necrotic myocardium, eventually leading to heart failure. The formation of the necrotic myocardium causes an inflammatory response and recruitment of myofibroblasts, resulting in the formation of scar tissue and decreased function. Current treatment (excluding heart transplantation) aims to prevent further loss of cardiomyocytes, but cannot

To dissect out the role of hTBM expression for extending the cardiac xenograft survival, three xenografts from donor pigs not expressing (GTKO.CD46) were transplanted in SPF baboons using previously used anti-CD40 (2C10R4) antibody based immunosuppression. All heterotopic cardiac xenotransplantation’s were done without any technical difficulty or perioperative complications. Transplanted recipient baboons were successfully extubated immediately following surgery and were active, eating, and generally well soon after the operation. Use of left ventricular telemetry implant and serial echocardiograms confirmed vigorous xenograft contractility following transplantation. All the recipient baboons maintained their hemoglobin, hematocrit and RBC